Necrotizing soft tissue infections caused by Streptococcus pyogenes and Streptococcus dysgalactiae subsp. equisimilis of groups C and G in western Norway.

Streptococcus pyogenes (group A streptococcus, GAS) is a major cause of necrotizing soft tissue infection (NSTI). On rare occasions, other ß-haemolytic streptococci may also cause NSTI, but the significance and nature of these infections has not been thoroughly investigated. In this study, clinical and molecular characteristics of NSTI caused by GAS and ß-haemolytic Streptococcus dysgalactiae subsp. equisimilis of groups C and G (GCS/GGS) in western Norway during 2000-09 are presented. Clinical data were included retrospectively. The bacterial isolates were subsequently emm typed and screened for the presence of genes encoding streptococcal superantigens. Seventy cases were identified, corresponding to a mean annual incidence rate of 1.4 per 100 000. Sixty-one of the cases were associated with GAS, whereas GCS/GGS accounted for the remaining nine cases. The in-hospital case fatality rates of GAS and GCS/GGS disease were 11% and 33%, respectively. The GCS/GGS patients were older, had comorbidities more often and had anatomically more superficial disease than the GAS patients. High age and toxic shock syndrome were associated with mortality. The Laboratory Risk Indicator for Necrotizing Fasciitis laboratory score showed high values (≥6) in only 31 of 67 cases. Among the available 42 GAS isolates, the most predominant emm types were emm1, emm3 and emm4. The virulence gene profiles were strongly correlated to emm type. The number of superantigen genes was low in the four available GCS/GGS isolates. Our findings indicate a high frequency of streptococcal necrotizing fasciitis in our community. GCS/GGS infections contribute to the disease burden, but differ from GAS cases in frequency and predisposing factors.

Molecular epidemiological investigation of an outbreak of invasive beta-haemolytic streptococcal infection in western Norway.

During a decade-long, high endemic situation with severe group A streptococcal disease in western Norway, a cluster of 16 patients with invasive streptococcal disease was hospitalized during a period of 11 weeks. A study including clinical characteristics and molecular epidemiology of the outbreak was initiated. Relevant clinical information was obtained from the medical records of the patients. Nine of the 16 patients had soft tissue infection, and seven of these had streptococcal toxic shock syndrome (STSS). Mortality, both overall and among those with STSS, was 25%. Streptococcal isolates from these patients were characterized by serogrouping and emm sequence typing. The emm amplicons were further characterized by sequence analysis and restriction fragment length polymorphism (emm RFLP) analysis. The streptococci were identified as group A streptococcus (GAS) in 11 patients and group G streptococcus (GGS) in four patients. The patients with GGS infection were older than the patients with GAS infection, and all patients infected with GGS had predisposing comorbidities. Isolates from 13 patients were available for emm gene analysis and found to belong to nine different emm types. Similar differentiation was obtained with emm RFLP in GAS. Hence, the outbreak was polyclonal. Results suggestive of horizontal gene transfer and recombination between the emm genes of GAS, group C streptococcus and GGS were found in the isolates from seven patients. Such genetic recombination events suggest a possible role in pathogenesis.

[Outbreak of multiresistant Acinetobacter baumannii infection]. / Utbrudd av infeksjon med multiresistent acinetobacter baumannii.

BACKGROUND: Nosocomial infections caused by multiresistant gram-negative bacteria represent an increasing problem, especially among intensive care patients. A serious outbreak of infection caused by multi-resistant Acinetobacter baumannii occurred in four burn patients. Acinetobacter is a gram-negative coccibacilli which is widespread in nature, and has been reported as an increasing problem in critically ill patients. MATERIALS AND METHODS: The outbreak strain was introduced from Alicante, Spain, by a transferred patient. This strain was resistant to all commonly available systemic antibiotics (including the karbapenems and all aminoglycosides), and sensitive only to polymyxin B. Two patients were critically ill, one of them died in septic shock. RESULTS: The ward was closed for admission of new patients and hygiene precautions were strengthened. Extensive testing of staff and equipment revealed multi-resistant A baumannii on a shower trolley shared by several patients. The outbreak strain was also identified by restriction endonuclease analysis. The patients were kept strictly isolated until their burn wounds were sufficiently healed to allow them to be discharged to their homes. INTERPRETATION: Following discharge of the last patient and extensive cleaning and disinfection of the entire ward, the particularly resistant strain has not reoccurred. Still, this experience may warrant screening for multiresistant gram-negative rods in patients transferred from regions where broad resistance to antibiotics is a common problem.

Concentrations of cytokines in plasma of patients with large burns: their relation to time after injury, burn size, inflammatory variables, infection, and outcome.

OBJECTIVE: To monitor longitudinally the concentrations of cytokines in the plasma of patients with severe burns. DESIGN: Prospective open study. SETTING: Burns unit, university hospital, Norway. SUBJECTS: 27 patients (5 women and 22 men, mean age 37 (range 13-82) years). INTERVENTIONS: Measurement of plasma concentrations of interleukin-1beta(IL-1beta), interleukin-1 receptor antagonist (IL-1ra), interferon-7(IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) were measured by enzyme linked immunosorbent assays (ELISA). MAIN OUTCOME MEASURES: Changes in concentrations, and correlation with morbidity and mortality. RESULTS: The concentration of IL-1beta and IL-1ra were increased in all patients and highest at the time of admission. Initially there was little or no circulating IFN-gamma, but this increased from day 5-10 in all patients. Only 8/15 patients had transient increases in circulating TNF-alpha. Concentrations of IL-1ra correlated with total burn surface area (TBSA) and area of third degree burn, as well as with plasma concentrations of C - reactive protein (CRP). Concentrations of IL-1beta and IL-1ra were higher in patients who developed infective complications than in those who did not (interleukin-8 (IL-8) has previously been shown to follow this pattern as well). Patients who survived had significantly higher IL-1beta concentrations than those who died (13(1) compared with 3 (1) pg/ml, p = 0.005) CONCLUSION: There are significant time-dependent changes in plasma concentrations of IL-1beta, IL-1ra, IFN-gamma and TNF-alpha after serious burns. IL-1ra concentrations may be influenced by size of the burn and the acute phase response; IL-1beta, IL-1ra and IL-8 may have a role in the host's response to infection; and IL-1beta may influence outcome.

Impaired actin polymerization and depolymerization in neutrophils from patients with thermal injury.

Acquired neutrophil dysfunction is considered an important cause of increased susceptibility to infection in patients with burns. In the early postinjury phase, large amounts of circulating chemo-attractants, cytokines and endotoxins induce strong systemic activation of neutrophils which may impair their motile functions. Actin is the most prevalent component of the microfilament lattice that generates force for the neutrophil motile responses, and in the present study we examined the dynamics of actin polymerization and depolymerization in neutrophils from 11 patients with large burns. At admission, the amount of polymerized actin in unstimulated neutrophils was 39.9 per cent higher than that of parallel controls. In addition, there was a positive correlation between the amount of polymerized actin and the total body surface area (TBSA) burn. The time course of patient neutrophil actin polymerization in response to FMLP, C5a, (Ser-IL-8)72, (Ala-IL-8)77 and crosslinking of surface Fc gamma RII was similar to that of controls, and the maximal amount of neutrophil F-actin was demonstrated after 30 s stimulation. At the peak of actin polymerization, however, patient neutrophils contained 27.3, 24.0, 24.7 and 25.6 per cent more polymerized actin than control cells stimulated with FMLP, (Ser-IL,-8)77, (Ala-8)77 and Fc gamma RII crosslinking, respectively. However, the relative increase of neutrophil F-actin following stimulation was significantly lower in patients than in controls. Moreover, the rate of patient neutrophil actin depolymerization was 39.0, 23.5, 63.3 and 51.7 per cent lower than that of controls after stimulation with FMLP, C5a (Ser-IL-8)72 and Fc gamma RII crosslinking, respectively. At discharge, the dynamics of neutrophil actin polymerization and depolymerization were similar to that of controls. The results demonstrate that in neutrophils during the early postburn phase, there are increased basal levels of polymerized actin, a lower responsiveness to stimulation and a reduced rate of actin depolymerization. As periodic polymerization and depolymerization of actin is essential for all neutrophil motile responses, it is probable that the alterations observed may contribute significantly to the overall neutrophil dysfunction following thermal injury.